High glucose-induced upregulation of Rho/Rho-kinase via platelet-derived growth factor receptor-beta increases migration of aortic smooth muscle cells (Q28567946)

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English	High glucose-induced upregulation of Rho/Rho-kinase via platelet-derived growth factor receptor-beta increases migration of aortic smooth muscle cells	scientific journal article

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PubMed publication ID

31 January 2017

High glucose-induced upregulation of Rho/Rho-kinase via platelet-derived growth factor receptor-beta increases migration of aortic smooth muscle cells (English)

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PubMed publication ID

31 January 2017

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Noboru Akiyama

1

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31 January 2017

Keiko Naruse

2

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Yasuko Kobayashi

3

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31 January 2017

Nobuhisa Nakamura

4

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31 January 2017

Yoji Hamada

5

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Eitaro Nakashima

6

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31 January 2017

Tatsuaki Matsubara

7

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Yutaka Oiso

8

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31 January 2017

Jiro Nakamura

9

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31 January 2017

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1 August 2008

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31 January 2017

Journal of Molecular and Cellular Cardiology

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31 January 2017

45

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2

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326–332

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31 January 2017

Heart failure: the frequent, forgotten, and often fatal complication of diabetes

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Chimera analysis supports a predominant role of PDGFRbeta in promoting smooth-muscle cell chemotaxis after arterial injury

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Insulin and local growth factor PDGF induce intimal hyperplasia in bypass graft culture models of saphenous vein and internal mammary artery

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Signalling mechanisms in the regulation of vascular cell migration

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Diabetes mellitus induces accelerated growth of aortic smooth muscle cells: association with overexpression of PDGF beta-receptors

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Glucose-induced hyperproliferation of cultured rat aortic smooth muscle cells through polyol pathway hyperactivity

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Glucose-induced phosphatidylinositol 3-kinase and mitogen-activated protein kinase-dependent upregulation of the platelet-derived growth factor-beta receptor potentiates vascular smooth muscle cell chemotaxis.

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Atherosclerosis — An Inflammatory Disease

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Rho signals to cell growth and apoptosis

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Formation of actin stress fibers and focal adhesions enhanced by Rho-kinase

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Recent evidence for an involvement of rho-kinase in cerebral vascular disease

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Inhibition of RhoA/Rho kinase pathway is involved in the beneficial effect of sildenafil on pulmonary hypertension

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In vivo gene transfer of dominant-negative rho-kinase induces regression of coronary arteriosclerosis in pigs.

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Fasudil, a Rho-kinase inhibitor, attenuates angiotensin II-induced abdominal aortic aneurysm in apolipoprotein E-deficient mice by inhibiting apoptosis and proteolysis

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Diabetes in the Goto-Kakizaki rat is accompanied by impaired insulin-mediated myosin-bound phosphatase activation and vascular smooth muscle cell relaxation

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Human proinsulin C-peptide prevents proliferation of rat aortic smooth muscle cells cultured in high-glucose conditions

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Oncogenic Ras downregulates Rac activity, which leads to increased Rho activity and epithelial-mesenchymal transition

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The pathogenesis of atherosclerosis--an update

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Enhanced arterial intimal thickening after balloon catheter injury in diabetic animals accompanied by PDGF beta-receptor overexpression of aortic media

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Rho-Rho kinase is involved in smooth muscle cell migration through myosin light chain phosphorylation-dependent and independent pathways

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Contribution of Rho A and Rho Kinase to Platelet-Derived Growth Factor-BB-Induced Proliferation of Vascular Smooth Muscle Cells

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Different migration of vascular smooth muscle cells from human coronary artery bypass vessels. Role of Rho/ROCK pathway

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A small GTP-binding protein, Rho, associates with the platelet-derived growth factor type-beta receptor upon ligand binding.

1 reference

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Upregulation of small GTPase RhoA in the basilar artery from diabetic (mellitus) rats

1 reference

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Increased expression and activity of RhoA are associated with increased DNA synthesis and reduced p27(Kip1) expression in the vasculature of hypertensive rats

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Imatinib mesylate--a new oral targeted therapy

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Reversal of experimental pulmonary hypertension by PDGF inhibition

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7 January 2021

Identifiers

10.1016/J.YJMCC.2008.04.006

1 reference

PubMed publication ID

31 January 2017

PubMed publication ID

1 reference

PubMed publication ID

31 January 2017

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